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Posterior Segment > Block 16 Vitreoretinal, Retinal, and Choroidal Dystrophies > Flashcards

Block 16 Vitreoretinal, Retinal, and Choroidal Dystrophies Flashcards

1
Q

Hereditary, metabolic diseases that involve the retina and affect both eyes are known as ____?

A

Retinal dystrophies

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2
Q

Retinal dystrophies primarily affect which region/layer of the retina?

A

Outer retina - photoreceptors and RPE

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3
Q

What is the most common hereditary fundus disorder?

A

Retinitis pigmentosa

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4
Q

What is more defective in Retinitis Pigmentosa, rods or cones?
What kind of dystrophy is this classified as?

A
  • Rods more defective

- “Rod-cone Dystrophy”

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5
Q

What does it mean if a retinal dystrophy is classified as a “Cone-Rod Dystrophy”

A

Cones more defective/affected than rods

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6
Q

Is typical or atypical Retinitis Pigmentosa more likely to be associated with a systemic condition?
What is the most common systemic association?

A
  • Atypical

- Usher’s Syndrome

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7
Q

What is the presenting symptom in typical retinitis pigmentosa?

A

Nyctalopia (night-blindness)

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8
Q

Most patients with typical retinitis are symptomatic by what age?

A

30

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9
Q

What is the classic triad of fundus changes in typical retinitis pigmentosa?

A
  1. Retinal “bone-spicule” changes
  2. Narrowing of retinal arterioles (attenuation)
  3. Waxy optic disc pallor
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10
Q

What are 3 possible presentations of atypical retinitis pigmentosa?

A
  1. RP Sine Pigmento
  2. Sector RP
  3. Retinitis punctata albescens
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11
Q

Scattered whitish spots, mostly near equator refers to which type of atypical RP?

A
  • Retinitis Punctata Albescens
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12
Q

Pigmentary changes in only a quadrant or 2 refers to which type of atypical RP?
Which quadrant is most commonly involved?

A
  • Sector RP

- Inferior quadrant

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13
Q

Peripheral lipid deposition in retinitis pigmentosa indicates early or late stage?

A

Late

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14
Q

Exudative retinal detachment in retinitis pigmentosa indicates early or late stage?

A

Late

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15
Q

What type of cataract is more common in all types of retinitis pigmentosa?

A

Posterior subcapsular cataract

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16
Q

What type of refractive error is common in retinitis pigmentosa?

A

Myopia

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17
Q

How is the optic nerve often affected in retinitis pigmentosa?

A

Optic nerve drusen

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18
Q

Retinitis pigmentosa may be associated with an early or late PVD (post. vitreous detachment)?

A

Early PVD in retinitis pigmentosa

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19
Q

Peripheral lipid deposition and exudative retinal detachment in retinitis pigmentosa is similar to what other disease?

A

Coat’s disease

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20
Q

Hearing loss + retinitis pigmentosa is known as ___

A

Usher’s Syndrome

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21
Q

Most systemic associations with retinitis pigmentosa are _____ disorders?

A

Metabolic disorders

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22
Q

What disease accounts for 50% of blind and deaf individuals?

A

Usher’s Syndrome

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23
Q

Where is a scotoma found initially in retinitis pigmentosa?

A

Mid-peripheral

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24
Q

How is an ERG affected by retinitis pigmentosa?

A

Scotopic function reduced early and extinguished late

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25
Q

Is dark adaptation shortened or prolonged in retinitis pigmentosa?

A

Prolonged

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26
Q

How can associated CME be treated in retinitis pigmentosa?

A

Oral acetazolamide

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27
Q

What is the most effective treatment for retinitis pigmentosa?

A

No universally effective treatment

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28
Q

A genetic disorder that affects both rods and cones from birth is known as ___?

A

Leber’s Congenital Amaurosis

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29
Q

What do parents often notice in a newborn that causes them to seek care in Leber’s Congenital Amaurosis?

A

Wandering eyes

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30
Q

How are pupils affected in Leber’s Congenital Amaurosis?

A

Little or no response to light

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31
Q

How is the fundus affected initially in Leber’s Congenital Amaurosis?

A

May appear normal initially

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32
Q

Is Leber’s Congenital Amaurosis bilateral or unilateral?

A

Bilateral

ALL retinal dystrophies are bilateral

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33
Q

Is an ERG affected in Leber’s Congenital Amaurosis?

A

Severly reduced or extinguished

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34
Q

Oculodigital syndrome can lead to _____ in Leber’s Congenital Amaurosis

A

Enophthalmos

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35
Q

What are 4 ocular changes over time in Leber’s Congenital Amaurosis?

A
  1. Progressive narrowing of retinal arterioles
  2. RPE degeneration
  3. Macular pigmentation or atrophy
  4. Optic nerve atrophy
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36
Q

Oculodigital syndrome leading to enophalmos is a sign of ____

A

Leber’s Congenital Amaurosis

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37
Q

Synthesis of _____ is abnormal in Albinism?

A

Melanin

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38
Q

What is it called if a genetic disorder with abnormal melanin synthesis affects the eyes, skin and hair?

A

Oculocutaneous albinism

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39
Q

What enzyme is affected in Albinism?

A

Tyrosinase

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40
Q

How is ocular albinism inherited?

A

X-linked

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41
Q

Which type of albinism has no melanin production at all throughout the body?

A

Oculocutaneous Albinism - Tyrosinase negative (complete)

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42
Q

Which type of albinism has reduced melanin production throughout the body?

A

Oculocutaneous Albinism - Tyrosinase positive (incomplete)

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43
Q

Are males or females more commonly affected with ocular albinism?

A

Males (x-linked inheritance)

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44
Q

What signs do female carriers of ocular albinism show?

A

Little to no ocular changes

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45
Q

What signs do males with ocular albinism show?

A

Iris and fundus hypo pigmentation

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46
Q

A newborn with little to no response to light in both pupils most likely has _____

A

Leber’s Congenital Amaurosis

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47
Q

Is ocular albinism usually bilateral or unilateral?

A

Bilateral

ALL retinal dystrophies involve both eyes!

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48
Q

Why is VA reduced in ocular albinism?

A

Foveal hypoplasia

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49
Q

What type of refractive error is common in ocular albinism?

A

High - myopia or hyperopia

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50
Q

Reduced or absent stereopsis + fundus showing variable choroidal vessels bilaterally is most likely _____

A

Ocular Albinism

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51
Q

What test can be used to show tyrosinase activity?

A

Hair bulb incubation after age 5

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52
Q

What is a patient with ocular albinism at increased risk for?

A

Basal cell carcinoma and squamous cell carcinoma

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53
Q

The most common genetic cause of vision loss in infants and children is _____

A

Leber’s Congenital Amaurosis

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54
Q

What common complaint/symptom may require special lenses in Ocular Albinism?

A

Photophobia (tinted lenses)

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55
Q

When are hematologic consultations indicated in albinism?

A

Tyrosinase positive

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56
Q

An important component for normal eye function that is defective in ocular albinism is _____

A

Melanin

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57
Q

What is the most common macular dystrophy?

A

Stargardt’s Disease

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58
Q

What is the most common hereditary fundus disorder?

A

Retinitis Pigmentosa

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59
Q

A patient with a hypopigmented fundus and iris + have light skin that can sometimes darken most likely has ______?
Which form?

A
  • Oculocutaneous Albinism

- Tyrosinase positive (incomplete)

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60
Q

Stargardt’s disease occurs due to _______?

A

Abnormal accumulation of lipofuscin within RPE

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61
Q

How is vision affected in Stargardt’s disease?

A

Gradual impairment of vision in children

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62
Q

When might Stargardt’s disease not be discovered until adult eye exam?

A

If macula is not involved and therefore vision not impaired

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63
Q

Initially, the fundus appears ______ in Stargardt’s disease.

A

Normal

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64
Q

How does the appearance of the macula progress in Stargardt’s disease?

A

Beaten bronze appearance, then bulls eye atrophy

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65
Q

What appears at posterior pole in Starboard’s disease?

A

Light colored flecks

66
Q

What does “fundus flavimaculatus” mean?

A

Light colored flecks that extend to mid-periphery without significant macular changes

67
Q

Patients affected with ______ are at increased risk for basal or squamous cell carcinoma.

Does the condition affect one or both eyes?

A
  • Albinism

- Both eyes (retinal dystrophy!!)

68
Q

What is a characteristic finding with fluorescein angiography in Stargardt’s Disease?

A

“dark choroid” overall, with window defect at macula

69
Q

When does visual loss tend to accelerate in Stargardt’s Disease?

A

When it reaches 20/40

70
Q

When does vision loss tend to stabilize in Stargard’ts Disease?

A

20/200

71
Q

How is EOG affected in Stargardt’s Disease?

A

Abnormal in advanced disease

72
Q

What is the characteristic appearance of fundus autofluorescence in Stargardt’s Disease?

A

Macular hypoautofluorescence with surrounding hyperautofluorescent flecks

73
Q

What can develop in Stargardt’s Disease and have devastating effect on vision?

A

CNV (choroidal neovascularization)

74
Q

A genetic disorder that affects primarily cones is ________?

A

Progressive cone dystrophy

75
Q

Progressive cone dystrophy universally leads to _____?

A

Severe central vision loss (20/200 or worse)

76
Q

What symptom may follow vision loss in progressive cone dystrophy?

A

Photophobia

77
Q

Gradual deterioration of _______ in progressive cone dystrophy? (2 answers)

A

Central vision and Color vision

78
Q

Progressive cone dystrophy typically presents in what age group?

A

Teens or young adults

79
Q

Describe appearance of macula initially in progressive cone dystrophy

A

Normal

80
Q

How does the appearance of the macula progress in progressive cone dystrophy?

A

Normal –> Bulls eye –> geographic atrophy

81
Q

Retinitis pigmentosa is the most common ______

A

Hereditary fundus disorder

82
Q

How could RPE changes be detected before clinical signs in progressive cone dystrophy?

A

Fluorescein angiography

83
Q

Annular changes surrounding fovea in Stargardt’s disease can be displayed by ____?

A

Fundus autofluorescence

84
Q

A non-progressive genetic disorder that is characterized by defective night vision is ______

A

Congenital Stationary Night Blindness

85
Q

List 3 potential appearances of fundus in Congenital Stationary night blindness.

A
  1. Normal
  2. Abnormal: Oguchi disease
  3. Abnormal: Fundus albipunctatus
86
Q

What condition may be associated with fundus flavimaculatus?

A

Stargardt’s Disease

87
Q

Golden yellow fundus in light adapted state that becomes normal after prolonged dark adaptation describes _____?

A

Oguchi disease in Congenital Stationary Night Blindness

88
Q

How is vision affected in fundus albipunctatus?

A

Functional impairment limited to scotopic vision only. Normal VA’s good

89
Q

Fundus with tiny yellow/white spots at posterior pole that extend into periphery + normal blood vessels, optic disc, and peripheral fields describes _____

A

Fundus albipunctatus in Congenital Stationary Night Blindness

90
Q

Deposition of crystals in retina and superficial peripheral cornea is _______

A

Bietti’s Crystalline Dystrophy

91
Q

A possible cause of Betti’s crystalline dystrophy is ____?

A

Error in systemic lipid metabolism

92
Q

An early sign of Bietti’s crystalline dystrophy is ____

A

fine yellow/white crystals scattered throughout posterior fundus

93
Q

A sign of progression of Bietti’s crystalline dystrophy is _____

A

Localized atrophy of RPE and choriocapillaris at macula –>
Diffuse atrophy of choriocapillaris + decrease in size and number of crystals –>
gradual confluence and expansion of atrophy –>
Chorioretinal atrophy (end stage)

94
Q

Hypofluorescent patches on fluorescein angiography corresponds to ____

A

Choriocapillaris loss and intact overlying retinal vessels

95
Q

Stargardt’s Disease is the most common _______

A

macular dystrophy

96
Q

Visual fields are constricted in ______ dystrophy that possibly involves an error in systemic lipid metabolism?

A

Bietti’s Crystalline Dystrophy

97
Q

Mutations in several genes that encode certain forms of Type 4 collagen can result in _______

A

Alport Syndrome

98
Q

Type 4 collagen is a major ________ component.

A

Basement membrane

99
Q

Chronic renal failure + deafness are common characterizations of which retinal dystrophy?

A

Alport Syndrome

100
Q

Fundus albipunctatus is associated with ______?

Fundus flavimaculatus is associated with _____?

A

Albipunctatus: Congenital stationary night blindness

Flavimaculatus: Stargardt’s disease

101
Q

How is an ERG affected in Alport Syndrome?

A

Normal

102
Q

Scattered, subtle yellow flecks in perimacular area with larger peripheral flecks describes the appearance of _____?
Is this unilateral or bilateral?

A

Alport syndrome

Bilateral - all retinal dystrophies bilateral!

103
Q

An asymptomatic condition with numerous diffusely distributed yellow/white polymorphous lesions that spare fovea and spread to far periphery is most likely _____

A

Familial benign fleck retina

104
Q

The flecks seen on the fundus in familial benign fleck retina are probably composed of _____?

A

Lipofuscin

105
Q

The second most common macular dystrophy is?

A

Best’s (Vitelliform) Macular Dystrophy

106
Q

FA showing “dark choroid” overall, with window defect at macula

A

Stargardt’s disease

107
Q

A genetic disorder in which an RPE lesion at the posterior pole eventually disrupts the macula is known as ____?

A

Best’s (Vitelliform) Macular Dystrophy

108
Q

An asymptomatic condition with numerous diffusely distributed yellow/white polymorphous lesions that spare fovea and spread to far periphery has what inheritance pattern?

A

Autosomal recessive

Familial benign fleck retina

109
Q

What are symptoms of Best’s macular dystrophy in early stages?

A

Asymptomatic in early stages

110
Q

Anterior lenticonus and posterior polymorphous corneal dystrophy may be associated with which retinal dystrophy?

A

Alport Syndrome

111
Q

When does vision become impaired in Best’s macular dystrophy?
What signs are associated with this stage?

A
  • Vitelliruptive Stage

- Lesion breaks up and forms “scrambled egg” appearance

112
Q

What is the first sign seen in Best’s macular dystrophy?

What stage is this associated with?

A
  • Egg-yolk lesion in early childhood made of excessive lipofuscin-like material
  • Vitelliform stage
113
Q

Partial reabsorption of a lesion around puberty is a common sign of _________ (overall disease) during ________ stage.

A
  • Best’s Vitelliform Macular Dystrophy

- Pseudohypopyon stage

114
Q

What symptom occurs when the lesion breaks up and forms “scrambled egg” appearance in Best’s macular dystrophy?

A

Impaired vision

115
Q

End-stage disease is classified under what stage of Bests macular dystrophy?

A

Atrophic stage

116
Q

When does the lesion disappear in best’s macular dystrophy? What is left behind?

A
  • Atrophic stage

- Atrophic macula left behind

117
Q

What type of cells/layer of retina is involved in Best’s Macular Dystrophy?

A

RPE

118
Q

What age does atrophic stage of Best’s macular dystrophy usually occur?

A

Middle age

119
Q

Eventual loss of central vision in Best’s macular dystrophy is due to ____

A

Geographical atrophy and/or subretinal fibrosis/scarring

120
Q

What can occur with subretinal fibrosis/scarring in Best’s macular dystrophy?

A

CNV

121
Q

How is EOG affected in Best’s macular dystrophy?

A
  • Abnormal in all stages

- Even abnormal in carriers of disease with normal fundus

122
Q

How is ERG affected in Best’s macular dystrophy?

A

Normal

123
Q

What should be provided for patient’s to take home with them if they have Best’s macular dystrophy

A

Amsler grid

124
Q

Vitelliform lesions refer to what characteristic appearance?

A

Egg-yolk

125
Q

Are lesions single or multifocal in Best’s Vitelliform Macular Dystrophy?

A

Single

126
Q

What age does Best’s vitelliform macular dystrophy typically present in?

A

Childhood, and progresses throughout middle age

127
Q

Multi-focal egg-yolk lesions seen in adults is ______ and their EOG is _______ and family history is ______

A
  • Vitelliform lesions without best’s disease
  • normal EOG
  • no family history
128
Q

A group of related genetic diseases of RPE that display various distinct patterns of lipofuscin deposits within the macula are known as ____

A

Pattern dystrophies

129
Q

How does the egg-yolk lesion in adult-onset macular vitelliform dystrophy differ from best’s? (2 answers)

A
  • Lesion is smaller in adult-onset (less than 1/2 disc diameter)
  • Lesion does not progress through typical stages or result in macular atrophy
130
Q

What are the 5 stages of Best’s macular dystrophy?

A
  1. Pre-Vitelliform
  2. Vitelliform
  3. Pseudohypopyon
  4. Vitelliruptive
  5. Atrophy
131
Q

A single egg-yolk lesion that presents in adulthood is most likely a _______ (type of condition, not specific name)

A

Pattern dystrophy

132
Q

How are ERG’s affected in pattern dystrophies?

A

Normal

133
Q

What is the most common pattern dystrophy?

A

Butterfly macular dystrophy

134
Q

A tri-radiate or spoke-like patterned lesion with a rim of RPE atrophy surrounding it is most likely composed of _____? And is called?

A
  • Composed of lipofuscin

- Butterfly macular dystrophy

135
Q

What test shows the RPE atrophy in Butterfly macular dystrophy?

A

Fluorescein angiography

136
Q

Fundus flavimaculatus that appears in adulthood and does not have a “dark choroid” with fluorescein angiography is most likely associated with _____?

A

Pattern dystrophy simulating fundus flavimaculatus

137
Q

What is fundus flavimaculatus?

A

light colored flecks that appear at macular pole and extend to mid-periphery without significant macular changes

138
Q

Why does pattern dystrophy simulating fundus flavimaculatus not have a dark choroid appearance with fluorescein angiography, like it does in _______ disease?

A
  • Because it is a pattern dystrophy and therefore the lipofuscin deposits are only affecting RPE at macula
  • Stargardt’s disease
139
Q

A genetic disorder that leads to early-onset accumulation of macular drusen is ______?

A

Familial dominant drusen

140
Q

When does accumulation of macular drusen typically begin in familial dominant drusen? When does it become symptomatic?

A
  • Begins in teens

- Symptomatic at 30-40

141
Q

What causes eventual vision impairment in familial dominant drusen?

A

RPE degeneration/geographical atrophy. And occasionally CNV

142
Q

Drusen that becomes more numerous with “honeycomb” appearance is characteristic of _____?

A

Familial dominant drusen

143
Q

How is ERG affected in Familial dominant drusen?

A

normal

144
Q

How is EOG affected in familial dominant drusen?

A

Subnormal in advanced disease

145
Q

Central areolar choroidal dystrophy is a genetic disease characterized by slowly expanding macular atrophy without _____? (2 answers)

A
  1. Lipofuscin

2. Drusen

146
Q

Fundus changes are limited to what area of the retina in central areolar choroidal dystrophy?

A

Macula

147
Q

List 3 signs of progression in central areolar choroidal dystrophy

A
  1. Begins as pigmentary change at fovea
  2. Well-circumscribed area of RPE and choriocapillaris loss at macula
  3. Geographic atrophy
148
Q

When is central vision impairment first noticed in central areolar choroidal dystrophy?
When does it become severe?

A
  • First noticed at young adult

- Severe by 50-70

149
Q

How is the appearance of drusen described in familial dominant drusen?

A

Honeycomb

150
Q

A genetic condition that involves central macular defects present at birth that rarely progress is most likely ____

A

North Carolina Macular Dystrophy

151
Q

Are fundus findings better or worse than expected based on a patient’s VA’s with North Carolina Macular Dystrophy?

A

Fundus findings are more significant than expected

152
Q

How common is north carolina macular dystrophy?

A

Rare

153
Q

When do macular defects first appear in north carolina macular dystrophy?

A

Present at birth

154
Q

Grade 1 north carolina macular dystrophy has what signs?

A

Fine druses-like deposits within RPE at macula

155
Q

Grade 2 north carolina macular dystrophy has what signs?

A

Larger confluent deposits at macula

156
Q

Grade 3 north carolina macular dystrophy has what signs?

A

Well-defined macular chorioretinal atrophy (coloboma-like)

157
Q

A genetic disease with lack of drusen and lipofuscin in slowly expending macular atrophy is most likely ____

A

Central areolar choroidal dystrophy

158
Q

Fine druses-like deposits within RPE at macula is Grade 1, 2, or 3 north carolina macular dystrophy?

A

Grade 1

159
Q

Coloboma-like appearance is grade 1, 2, or 3 north carolina macular dystrophy?

A

Grade 3

160
Q

Does north carolina macular dystrophy affect one or both eyes?

A

Both

All retinal dystrophies affect both eyes!

Posterior Segment (5 decks)

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